Cigarette smoking is the leading cause of preventable disease and death in the U.S. It causes colorectal cancer, liver cancer, adverse health outcomes in cancer patients and survivors, heart disease, stroke, lung diseases, diabetes, orofacial clefts in infants, ectopic pregnancy, rheumatoid arthritis, and chronic obstructive pulmonary disease (COPD), which includes emphysema and chronic bronchitis. Smoking also increases risk for stroke, tuberculosis, certain eye diseases, and problems of the immune system, including rheumatoid arthritis. It is a known cause of erectile dysfunction in males as well.
According to the Centers for Disease Control and Prevention (CDC), smoking accounts for more than 480,000 deaths every year, or 1 of every 5 deaths. 41,000 of these deaths are from exposure to secondhand smoke.
Today, there are more than 16 million Americans who live with a smoking-related disease. In addition, smoking-related illness in the United States costs more than $300 billion a year, including nearly $170 billion in direct medical care for adults and $156 billion in lost productivity.
The good news is, smoking rates have gradually declined over the decades. Half a century ago, more than two of every five adults were smokers. But from 2005 to 2015, the adult smoking rate declined from 20.9% to 15.1%.
That’s a monumental achievement that we can all be proud of. However, 15.1% of the population still works out to an estimated 36.5 million adults in the U.S. Of these, 75.7% (27.6 million) smoke every day, and 24.3% (8.9 million) smoke some days.
Although public health officials are hoping to to drive that rate below 12% by 2020, more needs to be done on all fronts in order to get there. Programs and policies that have worked include raising the retail price of cigarettes and other tobacco products, smoke free indoor air policies, high-impact media campaigns, full access to cessation treatments, and funding of comprehensive statewide tobacco control programs at the CDC recommended levels.
Another strategy that needs to be employed is the development of new, more powerful, and more effective smoking cessation medications.
Cannabidiol could reduce cigarette consumption in tobacco smokers
Rimonabant, also known as SR141617, Acomplia, or Zimulti, was an appetite suppressant and anti-obesity drug that worked as an inverse agonist for the cannabinoid receptor CB1.
But researchers also discovered that the drug was more than just a one-trick pony. Rimonabant was found to reduce nicotine self-administration in rodents and block reinstatement of drug seeking behavior following withdrawal from nicotine. Because of its ability to regulate the endocannabinoid system, researchers were hoping it would prove to be a powerful new smoking cessation medication.
Unfortunately, even though Rimonabant was effective in treating obesity and showed promise for nicotine addiction, it was later discovered that the drug caused serious psychiatric side effectives including depressive disorders, mood alterations, and even suicidal ideation. It was eventually banned worldwide.
However, one of the key takeaways from the Rimonabant controversy was further proof that the endocannabinoid system was intrinsic to reward and reinforcement. In fact, studies have shown that the endocannabinoid system is involved in the common neurobiological mechanism underlying drug addiction – including the rewarding effects of drugs, the ‘hedonic experience’ users feel when taking drugs, and the relapse to drug-seeking behavior. Evidence also suggests that cannabidiol or CBD may be a useful treatment in addictive behaviors – including nicotine dependence.
For example, in a 2013 study published in the journal Addictive Behaviors, a group of researchers from the U.K. studied the impact of CBD use on smokers who wished to stop smoking. 24 smokers were randomized to receive an inhaler of CBD or placebo for one week and they were instructed to use the inhaler when they felt the urge to smoke.
The results showed that placebo treated smokers showed no differences in number of cigarettes smoked. However, the smokers who received the inhaler of CBD significantly reduced the number of cigarettes smoked by about 40% during treatment.
More importantly, even though cigarette use dropped by 40%, subjects did not report an increase in cravings. Given the pivotal role of craving in relapse, this is potentially very encouraging. The researchers felt the decrease in smoking observed may plausibly relate to the action of CBD at the CB1 receptor, given previous literature on similar reductions following treatment with Rimonabant. Another possible explanation is CBD’s role as an inhibitor of fatty acid amide hydroxylase (FAAH) – an enzyme that breaks down endocannabinoids like anandamide. FAAH inhibition has previously been shown to reduce the reinforcing and neurochemical effects of nicotine in rats.
CBD also seemed to reduce the salience (importance) of cues and may have weakened the attentional bias of smokers to smoking stimuli. Attentional bias is thought to play a fundamental role in maintaining the cycle of craving and relapse in addiction and therefore a reduction in salience of smoking cues would be predicted to have a powerful effect on substance use, as is seen in this study. CBD may have also disrupted reconsolidation – a memory process by which memories are destabilized which has been suggested to have a therapeutic role in addiction.
Because this was a small preliminary study, the results must be taken with a grain of salt. But nevertheless, the dramatic difference between the CBD inhaler and placebo suggests that CBD could be a potential treatment for nicotine addiction and warrants further exploration.
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